A very interesting lesson has been learned from observing combat related Traumatic Brain Injury (TBI). A review, coauthored by a researcher in Wuhan, describes how TBI includes both primary and secondary impairments. Iron overload and ferroptosis highly involved in the pathophysiological process of secondary brain injury. Ferroptosis is a form of regulatory cell death, as increased iron accumulation in the brain leads to lipid peroxidation, reactive oxygen species (ROS) production, mitochondrial dysfunction and neuroinflammatory responses, resulting in cellular and neuronal damage.

ACCELERATED AGING AFTER BRAIN INJURY

Traumatic brain injury (TBI) causes long-term structural and functional alterations to the brain. Some of

these changes are thought to be progressive in nature. It has also been determined that those with even mild head injuries are at an elevated risk for death for 15 years post injury.

The hallmark feature of ferroptosis is the iron-dependent accumulation of oxidatively damaged phospholipids (i.e., lipid peroxides). This is also a hallmark of SARS-CoV-2 (see image with (2)).